CASE 1
A 13-year-old Quarter Horse gelding used for American sport disciplines was referred for stranguria of 12 hours’ duration, with a suspect of intravesical mass.
At first clinical examination, the horse was bright and responsive, heart rate 36 bpm, respiratory rate 40 bpm, rectal temperature 37.8°C, normal gut sounds, congested mucous membranes with slightly prolonged capillary refill time (2”). The horse showed constant urine dripping from the penis and appeared to experience pain while walking. The owner reported a sudden increase of muscular masses in the last days. Rectal palpation and ultrasonography revealed distended urinary bladder with mucous and viscous hyperechogenic content, enlarged spleen, and no other abnormalities. Haematology and biochemistry revealed moderate anaemia (hematocrit 26.5%), moderate azotaemia, mild hyponatremia, and markedly elevated levels of creatinine kinase (1.750.000 UI). A diagnosis of myopathy was made, and genetic analysis sent for a panel of breed-associated disorders. They subsequently revealed a heterozygous genotype for MYHM (myosin-heavy chain myopathy) gene and immunosuppressive therapy based on dexamethasone intravenously (IV) at 0,06 mg/kg q24 h for 5 days followed by 1 mg/kg prednisolone PO q24 h, was then instituted. Treatment with aggressive fluid therapy was initiated in association with flunixin meglumine IV 1.1 mg/kg q24 h. The stranguria was ascribed to the unwillingness of the horse to assume urination position due to muscle pain. The bladder was catheterized during the first visit and 7 litres of dark urine with sand deposits were removed. Bladder was washed with sterile saline solution to remove sabulous detritus. Stranguria persisted in the following days of hospitalization, despite analgesic treatment, and blood clots in the urines were observed macroscopically. Ultrasound examination of the bladder revealed a heterogeneous hyperechogenic mass in ventral portion of the urinary bladder (Figure 1D). The ventrocaudal part of the wall appeared thickened (8.4 mm) and oedematous, the rest of the organ presented a normo-echogenic aspect. At cystoscopy, performed using a 160-cm flexible endoscopec, the bladder mucosa was hyperaemic with diffuse petechiation and deep ulcers appreciable in the ventral aspect of the organ (Figure 1A-B). Macroscopically, urine appeared dark brown to rose in colour, with mucous as well as mucosal fragments and blood clots in suspension. Urine culture was requested (which then yielded a E. coli sensitive to trimethoprim-sulfamethoxazole [TMS]) and an initial treatment with 15 mg/kg ampicillin IV q8 h and 25 mg/kg TMS PO q12 h was started. Despite clinical improvements, marked bleeding persisted for up to ten days from the bladder ulcer, with hematocrit gradually decreasing. Local application of CSP on the bladder mucosa where the ulcer was evident was attempted under endoscopic guidance. The CSP (5 g) was gently inserted into a catheter with 1.8mm outer diameter and 190cm lengthd, which was then passed through the working channel of the endoscope after bladder emptying. Bleeding from the ulcer was substantial and margins of the lesion were not identifiable for long time. The powder was air pushed through the catheter and immediately created a gel coating over the ulcerated mucosal area. Endoscope was retracted and urine production closely monitored, as we hypothesized that the haemostatic clot could move and generate obstruction to urine outflow. Bladder transrectal ultrasound appearance was also monitored daily in the following days. Frank bleeding stopped in 24 hours after CSP application. The horse did not show pain or stranguria at any time and continue to autonomously void the bladder with the expected frequency. Ultrasonographically, a hyperecogenic halo was evident in the ventral portion of the bladder which gradually decreased in size over the next 7 days, which was interpreted as the clot induced by CSP over the area of ulcerated mucosa, while the mucosa became hypertrophic (Figure 1C-E-F). Treatment with TMS was continued for additional 7 days, when urine cytology and culture were judged negative. A further ultrasonographic control performed 14 days after the end of antimicrobial treatment still identified an area of thickened mucosa (Figure 1G), in the absence of evidence of macro or microhaematuria and inflammation.